Abstract 920: Determining the role of Siglecs in macrophage mediated immune evasion in prostate cancer
Abstract Siglecs (sialic acid-binding immunoglobulin-like lectins) are a family of cell surface proteins that are mainly expressed in immune cells. Recent studies show that Siglecs play important roles in immune evasion for tumors. We previously reported that Siglec-7 and Siglec-9 contribute to immune evasion by interacting with their ligands in prostate cancer, and blocking these interactions inhibits prostate cancer tumor progression. Further, Siglec-7 and Siglec-9 are highly expressed in macrophages in metastatic human prostate tumors. However, how macrophages mediate immune evasion via Siglec-dependent pathways remains unknown. Here, we have found that Siglec-7 and Siglec-9 are expressed in monocyte-differentiated macrophages derived from peripheral blood mononuclear (PBMC) cells. We will further profile Siglec expression in macrophages derived from PBMC and tumor tissues from patients with prostate cancer. The Siglecs on macrophages will be modulated, and their function will be evaluated through in vitro and in vivo models. Our study will provide insight into understanding macrophage-mediated immune evasion through Siglec-dependent mechanisms. Citation Format: Nathan S. Lam, Ru M. Wen, James D. Brooks. Determining the role of Siglecs in macrophage mediated immune evasion in prostate cancer [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2025; Part 1 (Regular Abstracts); 2025 Apr 25-30; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2025;85(8_Suppl_1):Abstract nr 920.
Authors
- James D. Brooks (ORCID: https://orcid.org/0000-0003-4521-7505)
- Nathan Lam
- Ru Wen (ORCID: https://orcid.org/0000-0002-0745-4051)
Institutions
- Stanford University (US)
Publication Details
- Journal
- Cancer Research
- Published
- 2025-04-21
- DOI
- https://doi.org/10.1158/1538-7445.am2025-920
- Primary Topic
- Flavonoids in Medical Research
- Type
- article
- Field-Weighted Citation Impact
- 0.00